Chen L, Sica A L, Greenberg H, Scharf S M
Pulmonary and Critical Care Division, Long Island Jewish Medical Center, Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, New York 11042, USA.
Respir Physiol. 1998 Mar;111(3):257-69. doi: 10.1016/s0034-5687(98)00007-3.
The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.
在七只预先植入仪器、使用镇静剂使其麻痹并进行通气的猪身上，研究了在三种条件下低氧血症和高碳酸血症对周期性非阻塞性呼吸暂停急性心血管反应的影响：室内空气呼吸（RA）、补充氧气（O2）以及补充氧气和二氧化碳（CO2）。脑电图监测显示在任何条件下均未出现觉醒。RA呼吸暂停会使平均动脉压升高（MAP，从基线的95.9±4.5升至呼吸暂停后期的124.4±7.8托，P<0.01），左心室舒张末期压力、舒张末期和收缩末期心肌纤维长度以及全身血管阻力增加，但心输出量（CO，从3.09±0.34降至2.37±0.26升/分钟，P<0.01）、心率（HR，从115.1±7.5降至102.0±7.8次/分钟，P<0.01）和每搏输出量（SV，从29.6±0.7降至21.1±1.8毫升，P<0.01）降低。与RA呼吸暂停相比，O2呼吸暂停使HR下降幅度相似（从114.0±11.8降至105.4±8.7次/分钟，P<0.05），但MAP升高幅度较小（从94.5±1.8升至103.4±2.8托，P<0.01），前后负荷变量升高幅度也较小。O2呼吸暂停时CO和SV保持不变。与RA相比，CO2在基线时与更高的MAP、CO和HR相关，但呼吸暂停期间的心血管反应在方向和幅度上与O2呼吸暂停相似。我们得出结论，在该模型中，低氧血症是呼吸暂停期间升压反应的主要但非唯一决定因素。高碳酸血症无法解释在低氧血症消除时出现的升压反应。呼吸暂停期间的心率下降与低氧血症、高碳酸血症和升压反应无关。
